Objective To discuss the relationship between self-control and aggressive structure of middle school students.Methods Using Self-control Questionnaire,Aggressive Questionnaire and the Implicit Association Test(IAT)to test 298 middle school students.Results The effects of students'thought control,emotion control and behavior control related not remarkable on implicit aggression(r=-0.11,r=-0.07,r=-0.03,P>0.05),but remarkable on the explicit aggression(β=-0.232,β=-0.188,β=-0.231,P＜0.05).The moderating effect of implicit aggression to the relationship between self-control and explicit aggression is weakly(△R2=0.007,P>0.05).Conclusion Self-control has remarkable inhibitory action to the explicit aggression,and the inhibitory action will not be influenced by implicit aggression.

Objective To observe the therapeutic effect of ATP sensitive potassium channel opening agent nicorandil com‐bined with classical treatment drug metformin for treating type 2 diabetes nephropathy (T2DN ) .Methods Thirty patients with T2DN were selected and divided into the control group(14 cases) and the experimental group(16 cases) .The control group was giv‐en metformin 0 .25 g ,3 times daily for 26 consecutive weeks .The experiment group was given the same dose of metformin and nic‐orandil 5 mg ,3 times daily for 26 weeks .The fasting blood glucose ,total cholesterol ,triglycerides ,low‐density lipoprotein(LDL) , high density lipoprotein(HDL) ,blood urea nitrogen ,serum creatinine ,urine albumin ,IL‐6 and MMP‐9 levels before and after treat‐ment were measured in both groups .Results There was no statistically significant difference in fasting blood glucose level after treatment between the control group and the experimental group(P>0 .05);the LDL level after treatment in the experiment group was significantly lower than that in the control group with statistical difference(P<0 .05);blood urea nitrogen ,serum creatinine and urine albumin levels after treatment in the experimental group were significantly lower than those in the control group with sta‐tistical difference(P<0 .05);the levels of serum IL‐6 and MMP‐9 after treatment in the experiment group were significantly lower than those in the control group with statistical difference(P<0 .05) .Conclusion Metformin combined with nicorandil could delay the progression of T2DN .

OBJECTIVETo observe the difference in the analgesic effect on primary dysmenorrheal between acupuncture and sham acupuncture at Sanyinjiao (SP 6) during menstrual pain and evaluate the impact of psychological effect on acupuncture analgesia.

METHODSSixty subjects were randomized into an acupuncture group and a sham acupuncture group, 30 cases in each one. The conventional acupuncture and sham acupuncture were applied to Sanyinjiao (SP 6) on bilateral sides when menstrual pain began to attack and needles were retained for 30 min each time. Three menstrual cycles were required. The visual analogue scale (VAS) was adopted to determine the scores before and 0. 5 h, 1 h, 3 h, 6 h and 12 h after acupuncture during menstrual pain in each cycle separately.

RESULTSIn the acupuncture group, VAS score at each time point after acupuncture was reduced as compared with that at the previous one during menstrual pain in each menstrual cycle, indicating the significant difference (all P<0. 05). In the sham acupuncture group, the scores in 6 h and 12 h of acupuncture were reduced as compared with the previous one, indicating the significant difference (all P<0. 05). After acupuncture, VAS score at each time point in the acupuncture group was lower than that in the sham acupuncture group (all P<0. 05).

CONCLUSIONThe conventional acupuncture at Sanyinjiao (SP 6) achieves the significant analgesic effect on primary dysmenorrheal. The psychological placebo effect of sham acupuncture has no obvious impact on acupuncture analgesia.

Acupuncture Analgesia ; Acupuncture Points ; Acupuncture Therapy ; Adult ; Dysmenorrhea ; physiopathology ; therapy ; Female ; Humans ; Menstrual Cycle ; Placebo Effect ; Young Adult

Objective To study the effect of recombinant human edostatin on peritoneal angiogenesis in uremic peritoneal dialysis(PD) rats. Methods Forty male SD rats were randomly divided into 5 groups: normal control rats (group 1), renal failure without PD rats (group 2), rats dialyzed with 4.25% PD solution (group 3), rats dialyzed with 4.25% PD solution and received subcutaneous injection of recombinant human endostatin 10 mg/kg (group 4), rats dialyzed with 4.25% PD solution and received subcutaneous injection of recombinant human endostatin 40 mg/kg (group 5). Recombinant human endostatin was given every other day during peritoneal dialysis period, total 14 times. After regular PD for 28 days, tissue immunohistochemical staining and RT-PCR were used to detect the mRNA and protein expressions of VEGF and bFGF in peritoneal tissues of each group rats. Microvessel density (MVD) of peritoneum was detected and quantified with anti-CD34 immunohistochemical staining. Results The mRNA and protein of VEGF and bFGF were expressed in each group. Compared to group 1, the mRNA and protein expression of VEGF and bFGF were significantly up-regulated in group 2 and group 3 (all P＜0.05). Compared with group 3, the mRNA and protein expression of VEGF and bFGF were significantly downregulated in group 4 and group 5 (all P＜0.05). Compared with group 4, the mRNA and protein expression of VEGF and bFGF were significantly down-regulated in group 5 (all P＜0.05). The new microvascular vessels in group 1 showed little or none. Compared with group 1, MVD was significantly increased in group 2 and group 3 (P＜0.05). Compared with group 3, MVD was significantly decreased in group 4 and group 5 (all P＜0.05). Conclusions Recombinant human endostatin can effectively inhibit rat peritoneal neoangiogensis. Down-regulated expression of VEGF and bFGF in peritoneum may be one of the mechanisms of recombinant human endostatin inhibiting peritoneal angiogenesis.

This study was aimed to build up a diagnosis and treatment procedure of traditional Chinese medicine (TCM) for HIV/AIDS headache. Domestic and foreign articles correlated to HIV/AIDS headache diagnosed and treat-ed by TCM were summarized. The specialist questionnaire of clinical diagnosis and treatment standard operating pro-cedures of TCM for HIV/AIDS headache was designed by focus group discussions. And the national specialist ques-tionnaire survey was carried out twice. The results showed that the standard operating procedure of TCM clinical di-agnosis, treatment, nursing and therapeutic efficacy assessment for HIV/AIDS headache was preliminarily established. It was concluded that this regulation identified concept, etiology and pathogenesis of HIV/AIDS, established TCM standard diagnosis and treatment service. It also demonstrated features of propaganda and education, follow-ups, con-secutive diagnosis and treatment inside or outside the hospital.

ObjectiveTo explore the molecular mechanism of Qidi Tangshen prescription （QDTS） in regulating podocyte pyroptosis in diabetes nephropathy （DN）. MethodThrough in vivo experiment， db/db mice were divided into the model group， QDTS group （3.34 g·kg^-1）， valsartan capsule group （10.29 mg·kg^-1）， with db/m mice serving as the normal control. Each group consisted of 8 mice， and they underwent continuous intervention for 8 weeks. After the last administration， mice were euthanized， and kidney pathological changes were observed. Additionally， the expression levels of pyroptosis-related indicators， including NOD-like receptor protein 3 （NLRP3）， Gasdermin D protein （GSDMD）， and interleukin-1β （IL-1β） protein， were examined. Through in vitro experiment， mouse podocytes were divided into the normal glucose group （5.5 mmol·L^-1 glucose）， high glucose group （35 mmol·L^-1 glucose）， DMSO group （35 mmol·L^-1 glucose+200 mg·L^-1 DMSO）， and QDTS group （35 mmol·L^-1 glucose+200 mg·L^-1 QDTS freeze-dried powder）. After 48 hours of intervention， the expression levels of NLRP3， GSDMD， and IL-1β proteins were measured in podocytes. A drug-ingredient-target-disease interaction network for QDTS in the treatment of DN was constructed by network pharmacology methods. The key signaling pathways regulating podocyte pyroptosis were analyzed， and validation was conducted through in vivo and in vitro experiments. ResultCompared with normal group， glomerular hyperplasia and glomerular basement membrane thickening were observed in model group， and some segments were accompanied by obvious podocellular process fusion. The protein expressions of NLRP3， GSDMD and IL-1β in mouse kidney were increased， the protein expressions of mitogen-activated protein kinase 14 （MAPK14）， V-Rel reticuloendotheliosis virus oncogene homology A （RELA） and Caspase-8 in mouse kidney were increased （P<0.05）. Compared with model group， kidney pathological injury of mice in QDTS group was significantly reduced， and the expressions of NLRP3， GSDMD and IL-1β in kidney of mice in QDTS group and valsartan group were decreased （P<0.05）. The protein expressions of MAPK14， RELA and Caspase-8 in kidney of mice in QDTS group and valsartan group were decreased （P<0.05）. Network pharmacology results showed that there were 16 targets for QDTS to regulate DN cell pyrodeath， among which MAPK14， RELA and Caspase-8 were the key targets. Compared with normal glucose group， the protein expressions of NLRP3， GSDMD and IL-1β in high glucose group were increased （P<0.05）， and the protein expressions of MAPK14， RELA and Caspase-8 in mouse podocytes were increased （P<0.05）. Compared with high glucose group， the expressions of NLRP3， GSDMD and IL-1β in podocytes of mice in QDTS group were decreased （P<0.05）， and the expressions of MAPK14， RELA and Caspase-8 in podocytes of mice in QDTS group were decreased （P<0.05）. ConclusionQDTS reduces damage to DN podocytes， which is associated with its regulation of the MAPK14/RELA/Caspase-8 signaling pathway and inhibition of podocyte pyroptosis.

ObjectiveTo explore the mechanism of Qidi Tangshen prescription （QDTS） in alleviating podocyte injury and reducing urinary protein in diabetic nephropathy （DN）. MethodUsing network pharmacology methods， we collected the chemical components and targets of QDTS， as well as the targets related to DN. Subsequently， we constructed a "drug-ingredient-target-disease" network for QDTS in the treatment of DN to systematically elucidate the mechanism. The db/db mice were assigned into the model， QDTS （3.34 g·kg^-1）， and losartan capsules （10.29 mg·kg^-1） groups， and db/m mice served as the normal group. Each group consisted of 8 mice， and they underwent continuous intervention for 8 weeks. After the last administration， mice were euthanized， and the urinary albumin excretion rate （UAER） and renal pathological changes were measured and observed. The expression levels of protein kinase B1 （Akt1）， hypoxia-inducible factor-1 alpha （HIF-1α）， phosphorylated B-cell lymphoma-extra-large （p-Bcl-xl）， as well as autophagy-related indicators microtubule-associated protein 1 light chain 3 （LC3）， ubiquitin-binding protein p62 （p62）， and autophagy-related gene 6 homolog （Beclin1）， were determined. Furthermore， mouse podocytes were divided into the normal glucose （5.5 mmol·L^-1）， high glucose （35 mmol·L^-1）， DMSO （35 mmol·L^-1 glucose+200 mg·L^-1 DMSO）， and QDTS （35 mmol·L^-1 glucose+200 mg·L^-1 QDTS freeze-dried powder） groups. After 48 h of intervention， the protein levels of Akt1， HIF-1α， p-Bcl-xl， LC3， p62， and Beclin1 in podocytes were measured. ResultQDTS had 34 active components acting on 143 targets in the treatment of DN， and 55 targets were related to autophagy， in which Akt1， HIF-1α， and Bcl-xl were the key targets. Compared with the normal group， mice in the model group exhibited significantly increased UAER， glomerular hypertrophy， deposition of blue collagen fibers， thickening of the glomerular basement membrane， and noticeable fusion of podocyte foot processes in some segments. Furthermore， the modeling up-regulated the protein levels of p-Akt1， HIF-1α， and p62 and down-regulating the protein levels of p-Bcl-xl， LC3， and Beclin1 in the renal tissue （P<0.05）. Compared with the model group， QDTS and losartan decreased UAER （P<0.05） and alleviated the pathological damage in the renal tissue. Moreover， QDTS and losartan down-regulated the protein levels of p-Akt1， HIF-1α， and p62 and up-regulated the protein levels of p-Bcl-xl， LC3， and Beclin1 in the renal tissue （P<0.05）. In comparison to the normal glucose group， the high glucose group displayed up-regulated protein levels of p-Akt1， HIF-1α， and p62 and down-regulated protein levels of p-Bcl-xl， LC3， and Beclin1 in podocytes （P<0.05）. Compared with the high glucose group， QDTS down-regulated the protein levels of p-Akt1， HIF-1α， and p62 and up-regulated the protein levels of p-Bcl-xl， LC3， and Beclin1 in podocytes （P<0.05）. ConclusionQDTS alleviates podocyte damage and reduced urinary protein in DN by regulating the Akt1/HIF-1α/Bcl-xl signaling pathway， thereby enhancing podocyte autophagy.